Literature DB >> 14614232

A missense mutation (GGC[435Gly]-->AGC[Ser]) in exon 8 of the CYP11B2 gene inherited in Japanese patients with congenital hypoaldosteronism.

Isao Kuribayashi1, Hideaki Kuge, Romero Jovel Santa, Aldahoodi Ziyad Mutlaq, Naohito Yamasaki, Takashi Furuno, Akio Takahashi, Shoichi Chida, Toshiro Nakamura, Fumio Endo, Yoshinori Doi, Saburo Onishi, Yutaka Shizuta.   

Abstract

OBJECTIVES: To clarify the underlying molecular mechanism of corticosterone methyl oxidase type II (CMO II) deficiency, Japanese patients newly diagnosed with CMO II deficiency were investigated.
METHODS: We analyzed the patients' genomic DNA sequence on all 9 exons of the CYP11B2 gene. In addition, restriction fragment length polymorphism (RFLP) analysis and expression studies were performed.
RESULTS: The analysis showed that the patients homozygously retained a missense mutation, Gumacr;GC[435Gly]-->Aumacr;GC[Ser], in the CYP11B2 gene. Expression studies indicated that the steroid 18-hydroxylase/oxidase activities of the mutant enzyme were substantially reduced.
CONCLUSION: These results support the hypothesis that this mutation causes CMO II deficiency in the patients, and are in accordance with our theory that the partial loss of P-450(C18) activities causes CMO II deficiency. Copyright 2003 S. Karger AG, Basel

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Year:  2003        PMID: 14614232     DOI: 10.1159/000074041

Source DB:  PubMed          Journal:  Horm Res        ISSN: 0301-0163


  3 in total

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  3 in total

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